Notably, in patients with RP mutations, the mRNA for GATA1, a master hematopoietic transcription factor, is poorly translated, further exacerbating the impaired erythroid defect characteristic of DBA, which might be due to the fact that this mRNA has a higher threshold for initiation in comparison to other mRNAs [16]. This evidence concerns the gene GATA1 and Diamond-Blackfan anemia.